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A 63 year old woman who fell off her bicycle had a left temporal region head injury with evidence of initial loss of consciousness of 5 minutes and scalp excoriation of that area. On arrival at our hospital 30 minutes later she was alert and oriented. Cranial nerve functions, including extraocular motion and hearing function, were preserved. Pain and temperature sensations of the right side, including her face, showed a 70% decrease compared with the left side; however, position and vibration sensations were normal. Other neurological examinations, including motor function, coordination, and deep tendon reflex, were normal. The patient's only complaints were left temporal headache and right hemihypaesthesia.

Brain CT on admission showed a discrete and linear high density at the left ambient cistern without other intracranial lesions. On the next day CT showed an obscure low density lesion at the dorsolateral midbrain in addition to the previous lesion (figure).

Brain MRI, taken 3 days later, demonstrated an intraparenchymal lesion, at the surface of the left dorsolateral midbrain in high intensity on a T2 weighted image. The high intensity lesion corresponding to haematoma on CT was seen in the ambient cistern (figure). Taking both CT scans and MRI into consideration, this case was diagnosed as traumatic midbrain contusion.

The loss of pain and temperature sensation improved gradually and the patient was discharged 2 weeks later.

T2 weighted images 1 month later showed a more localised lesion in the same area. The coronal slices showed a high intensity lesion at the level of lower midbrain coinciding with the tentorium level, disclosed as a low line between the occipital lobe and the cerebellar hemisphere (figure).

The neurological deficits almost disappeared 6 months later.

Somatosensory impairment including pain is one of the most common complaints among patients with craniocervical injury. Responsible lesions for sensory impairment, detectable by neuroimaging studies, almost always accompany associated neurological deficits.12 To our knowledge, a selective injury at the spinothalamic or trigeminothalamic tracts due to closed head injury has not been highlighted in the neurological literature.

(A) CT on admission showed a discrete and linear high density at the left ambient cistern. (B) Axial T2 weighted image taken 3 days later showed an intraparenchymal lesion, at the left posterolateral midbrain in high intensity. (arrow) The margin was rather obscure. The high and low intensity lesion corresponding to haematoma on CT was seen in the ambient cistern in the axial image. (arrow head) Taking both CT scans and MRI, this case was diagnosed as traumatic midbrain contusion. (C) An axial T2 weighted image 1 month later demonstrated a more discrete lesion at the dorsolateral midbrain tegmentum (arrow). (D) A coronal image showed a discrete high intensity lesion at the level of the lower midbrain (arrow) coinciding with the level of the tentorium, which was shown in low line between the occipital lobe and cerebellar hemisphere. The distance between the tentorial margin and brain stem was shorter on the injured side.

The MR images in our case showed a discrete lesion at the left dorsolateral midbrain. Topographical study at this lower midbrain level showed that the lateral and ventral spinothalamic and ventral trigeminothalamic tracts pass at the surface of this level by carrying a superficial somatofacial sensory input.3 The lesion shown in our MR images seemed to be localised to these tracts. The medial leminiscus for the deep sensation and lateral leminiscus and nucleus of inferior colliculus associated with hearing function run ventral and dorsal to these tracts, respectively; which were seemingly spared in our patient.3 The topographical anatomy seemed to correspond to the neurological manifestations of our patient.

The mechanism of midbrain injury in our patient was speculated to be due to tentorial coup injury based on MR images. The location of contusion was at the lower dorsolateral midbrain, coinciding with the tentorial edge level. Initiation of injury was the surface of the midbrain; however, due to the proximity of the tentorial edge to the midbrain on the injured side, tentorial contact to the midbrain supposedly occurred more readily. Brain MRI findings support the anatomical features of this tentorial coup injury. This injury is not rare in patients with severe head injury, accompanied by other intracranial lesions, and is often caused by lateral displacement of the brain stem relative to the tentorium. It is influenced by congenital variation in the size and shape of the tentorial incisura.12 The brain stem of the patient with a narrow incisura is more vulnerable to the direct contusive effects than that of a patient with a wider incisura. Therefore, even in minor head injury, this mechanism may occur in patients preconditioned with narrow tentorial incisura, which may have been the case in our patient.

The concept of tentorial coup injury against the midbrain is not new.4 It usually accompanies various degrees of conscious disturbance and other long tract signs, sensory deficits as well as cerebellar and cranial nerve palsy due to the midbrain lesion or other associated intracranial lesions.1245 The clinical manifestation of our patient may represent one of the mildest forms of the midbrain contusion. Therefore, when we see a patient with post-traumatic sensory deficit, the possibility of this tentorial injury should be kept in mind even in minor head injury.

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